Beta-cell dysfunction, rather than insulin insensitivity, is the primary defect in familial type 2 diabetes

Lancet. 1986 Aug 16;2(8503):360-4. doi: 10.1016/s0140-6736(86)90052-8.

Abstract

Continuous infusion of glucose with model assessment was used to measure glucose tolerance, beta-cell function, and insulin sensitivity in 154 first-degree relatives of 55 patients with type-2 diabetes. The plasma glucose achieved at 1 h was normally distributed in normal control subjects, but 31 (20%) of relatives of type-2 diabetics had values above the normal distribution mean +2 SD. Insulin secretion, assessed from the first or second phase plasma-C-peptide responses, was significantly lower in the glucose-intolerant relatives than in normoglycaemic relatives of similar sex, age, and obesity. beta-cell function, estimated by means of model analysis, was severely impaired in the glucose-intolerant relatives but was not impaired in the normoglycaemic relatives (geometric mean 41% and 109% of normal beta-cell response, respectively). Reduced beta-cell function was found with all degrees of glucose intolerance, whereas only the more severely hyperglycaemic relatives had impaired insulin sensitivity. This suggests that the primary defect in familial type-2 diabetes is beta-cell dysfunction.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Blood Glucose / metabolism
  • C-Peptide / blood
  • Diabetes Mellitus, Type 2 / blood
  • Diabetes Mellitus, Type 2 / genetics*
  • Diabetes Mellitus, Type 2 / physiopathology
  • Female
  • Glucose Tolerance Test*
  • Humans
  • Infusions, Parenteral
  • Insulin / blood
  • Insulin Resistance*
  • Islets of Langerhans / physiopathology*
  • Male
  • Middle Aged

Substances

  • Blood Glucose
  • C-Peptide
  • Insulin